Possible role of rice bran extract in microglial modulation through PPAR-gamma receptors in alzheimer’s disease mice model
Alzheimer's Disease (AD), the most prevalent neurodegenerative disorder among elderly people, is ordinarily associated with progressive cognitive decline. Peroxisome proliferator-activated receptors-gamma (PPAR-γ) agonists can be targeted as a beneficial therapeutic strategy against AD. In the...
Gespeichert in:
| Veröffentlicht in: | Metabolic brain disease 2021-10, Vol.36 (7), p.1903-1915 |
|---|---|
| Hauptverfasser: | , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 1915 |
|---|---|
| container_issue | 7 |
| container_start_page | 1903 |
| container_title | Metabolic brain disease |
| container_volume | 36 |
| creator | El-Din, Shimaa Saad Abd Elwahab, Sahar Rashed, Laila Fayez, Salwa Aboulhoda, Basma Emad Heikal, Ola Ahmed Galal, Asmaa Fathi Nour, Zeinab A. |
| description | Alzheimer's Disease (AD), the most prevalent neurodegenerative disorder among elderly people, is ordinarily associated with progressive cognitive decline. Peroxisome proliferator-activated receptors-gamma (PPAR-γ) agonists can be targeted as a beneficial therapeutic strategy against AD. In the present study, we aimed to investigate the preventive and therapeutic effects of rice bran extract (RBE) as a possible PPAR-γ agonist on the microglial phenotype modulation in AD in mice compared to the effects of pioglitazone. This study included 64 adult male Swiss Albino mice divided into 8 groups, each group comprised 8 mice; control group, RBE group, lipopolysaccharide-induced neurodegeneration (a) (LPSa) group, (LPSb) group, RBE-preventive group (RBE + LPSa), pioglitazone-preventive group (PG + LPSa), RBE-treated group (RBE + LPSb), and pioglitazone-treated group (PG + LPSb). Cognitive functions were assessed by Y-maze and Morris water maze tests. The expression of PPAR-γ, CD45, arginase1, CD36, and CD163 genes was assessed by real time qPCR and the estimation of NF-kβ protein level was done by Western blot technique. Moreover, the assessment of Aβ42 and P-tau levels was performed by ELISA. Histopathological examination of brain tissues was performed for all the studied groups. Our results showed that RBE and pioglitazone could modulate microglial phenotype from M1 to M2 where they significantly decreased the expression of NF-κβ and the pro-inflammatory microglial marker (CD45) in parallel with increasing the expression of the anti-inflammatory microglial and phagocytic markers (arginase1, CD163, and CD36). In addition, RBE and pioglitazone significantly increased PPAR-γ expression and reduced Aβ42 deposition as well as p-tau protein levels. In conclusion, our study identified the possible role of PPAR-γ agonistic activity of RBE as a preventive and therapeutic agent in the treatment of the neuro-inflammation associated with AD. |
| doi_str_mv | 10.1007/s11011-021-00741-4 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_2572077287</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2572077287</sourcerecordid><originalsourceid>FETCH-LOGICAL-c375t-691871de79e1df8086c8ab4f26cdeea24c22744fa5769f97b2ec703119050bde3</originalsourceid><addsrcrecordid>eNp9kMtO3DAUhi1UBFPaF-iistR12uNL4mSJEJdKI3WEYG05zsmMURJP7UQCxILX6Ov1SXA6U9ixsL3w_39H5yPkC4PvDED9iIwBYxnwdEBJlskDsmC5EpkSRf6BLKAs80zJCo7JxxjvAEDkrDoix0KCFIwXC_K08jG6ukMafLp8S4OzSOtgBor3YzB2pG6gvbPBrztnOtr7ZurM6PxAx03w03pDV6vT62xt-t7QgBa3ow9xbpnucYOux_D3-U-kjYtoIs4snCnYfSKHrekift6_J-T24vzm7Cpb_rr8eXa6zKxQ-ZgVFSsVa1BVyJq2hLKwpallywvbIBouLedKytbkqqjaStUcrQLBWAU51A2KE_Jtx90G_3vCOOo7P4UhjdQ8VxyU4qVKKb5LpVVjDNjqbXC9CQ-agZ6F651wnYTrf8K1TKWve_RU99i8Vv4bTgGxC8T0NawxvM1-B_sCMmCNew</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2572077287</pqid></control><display><type>article</type><title>Possible role of rice bran extract in microglial modulation through PPAR-gamma receptors in alzheimer’s disease mice model</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>El-Din, Shimaa Saad ; Abd Elwahab, Sahar ; Rashed, Laila ; Fayez, Salwa ; Aboulhoda, Basma Emad ; Heikal, Ola Ahmed ; Galal, Asmaa Fathi ; Nour, Zeinab A.</creator><creatorcontrib>El-Din, Shimaa Saad ; Abd Elwahab, Sahar ; Rashed, Laila ; Fayez, Salwa ; Aboulhoda, Basma Emad ; Heikal, Ola Ahmed ; Galal, Asmaa Fathi ; Nour, Zeinab A.</creatorcontrib><description>Alzheimer's Disease (AD), the most prevalent neurodegenerative disorder among elderly people, is ordinarily associated with progressive cognitive decline. Peroxisome proliferator-activated receptors-gamma (PPAR-γ) agonists can be targeted as a beneficial therapeutic strategy against AD. In the present study, we aimed to investigate the preventive and therapeutic effects of rice bran extract (RBE) as a possible PPAR-γ agonist on the microglial phenotype modulation in AD in mice compared to the effects of pioglitazone. This study included 64 adult male Swiss Albino mice divided into 8 groups, each group comprised 8 mice; control group, RBE group, lipopolysaccharide-induced neurodegeneration (a) (LPSa) group, (LPSb) group, RBE-preventive group (RBE + LPSa), pioglitazone-preventive group (PG + LPSa), RBE-treated group (RBE + LPSb), and pioglitazone-treated group (PG + LPSb). Cognitive functions were assessed by Y-maze and Morris water maze tests. The expression of PPAR-γ, CD45, arginase1, CD36, and CD163 genes was assessed by real time qPCR and the estimation of NF-kβ protein level was done by Western blot technique. Moreover, the assessment of Aβ42 and P-tau levels was performed by ELISA. Histopathological examination of brain tissues was performed for all the studied groups. Our results showed that RBE and pioglitazone could modulate microglial phenotype from M1 to M2 where they significantly decreased the expression of NF-κβ and the pro-inflammatory microglial marker (CD45) in parallel with increasing the expression of the anti-inflammatory microglial and phagocytic markers (arginase1, CD163, and CD36). In addition, RBE and pioglitazone significantly increased PPAR-γ expression and reduced Aβ42 deposition as well as p-tau protein levels. In conclusion, our study identified the possible role of PPAR-γ agonistic activity of RBE as a preventive and therapeutic agent in the treatment of the neuro-inflammation associated with AD.</description><identifier>ISSN: 0885-7490</identifier><identifier>EISSN: 1573-7365</identifier><identifier>DOI: 10.1007/s11011-021-00741-4</identifier><identifier>PMID: 34043126</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Aged ; Agonists ; Alzheimer Disease - drug therapy ; Alzheimer Disease - metabolism ; Alzheimer's disease ; Animals ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; CD163 antigen ; CD36 antigen ; CD45 antigen ; Chemical compounds ; Cognitive ability ; Humans ; Inflammation ; Lipopolysaccharides ; Male ; Markers ; Metabolic Diseases ; Mice ; Microglia - metabolism ; Modulation ; Neurodegeneration ; Neurodegenerative diseases ; Neurology ; Neurosciences ; Oncology ; Original Article ; Oryza - metabolism ; Peroxisome proliferator-activated receptors ; Phagocytes ; Pharmacology ; Phenotypes ; Pioglitazone ; Plant Extracts - pharmacology ; PPAR gamma - agonists ; PPAR gamma - metabolism ; Proteins ; Receptors ; Rice bran ; Tau protein ; Thiazolidinediones - therapeutic use</subject><ispartof>Metabolic brain disease, 2021-10, Vol.36 (7), p.1903-1915</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021</rights><rights>2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.</rights><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-691871de79e1df8086c8ab4f26cdeea24c22744fa5769f97b2ec703119050bde3</citedby><cites>FETCH-LOGICAL-c375t-691871de79e1df8086c8ab4f26cdeea24c22744fa5769f97b2ec703119050bde3</cites><orcidid>0000-0002-6101-8402</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11011-021-00741-4$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11011-021-00741-4$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34043126$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>El-Din, Shimaa Saad</creatorcontrib><creatorcontrib>Abd Elwahab, Sahar</creatorcontrib><creatorcontrib>Rashed, Laila</creatorcontrib><creatorcontrib>Fayez, Salwa</creatorcontrib><creatorcontrib>Aboulhoda, Basma Emad</creatorcontrib><creatorcontrib>Heikal, Ola Ahmed</creatorcontrib><creatorcontrib>Galal, Asmaa Fathi</creatorcontrib><creatorcontrib>Nour, Zeinab A.</creatorcontrib><title>Possible role of rice bran extract in microglial modulation through PPAR-gamma receptors in alzheimer’s disease mice model</title><title>Metabolic brain disease</title><addtitle>Metab Brain Dis</addtitle><addtitle>Metab Brain Dis</addtitle><description>Alzheimer's Disease (AD), the most prevalent neurodegenerative disorder among elderly people, is ordinarily associated with progressive cognitive decline. Peroxisome proliferator-activated receptors-gamma (PPAR-γ) agonists can be targeted as a beneficial therapeutic strategy against AD. In the present study, we aimed to investigate the preventive and therapeutic effects of rice bran extract (RBE) as a possible PPAR-γ agonist on the microglial phenotype modulation in AD in mice compared to the effects of pioglitazone. This study included 64 adult male Swiss Albino mice divided into 8 groups, each group comprised 8 mice; control group, RBE group, lipopolysaccharide-induced neurodegeneration (a) (LPSa) group, (LPSb) group, RBE-preventive group (RBE + LPSa), pioglitazone-preventive group (PG + LPSa), RBE-treated group (RBE + LPSb), and pioglitazone-treated group (PG + LPSb). Cognitive functions were assessed by Y-maze and Morris water maze tests. The expression of PPAR-γ, CD45, arginase1, CD36, and CD163 genes was assessed by real time qPCR and the estimation of NF-kβ protein level was done by Western blot technique. Moreover, the assessment of Aβ42 and P-tau levels was performed by ELISA. Histopathological examination of brain tissues was performed for all the studied groups. Our results showed that RBE and pioglitazone could modulate microglial phenotype from M1 to M2 where they significantly decreased the expression of NF-κβ and the pro-inflammatory microglial marker (CD45) in parallel with increasing the expression of the anti-inflammatory microglial and phagocytic markers (arginase1, CD163, and CD36). In addition, RBE and pioglitazone significantly increased PPAR-γ expression and reduced Aβ42 deposition as well as p-tau protein levels. In conclusion, our study identified the possible role of PPAR-γ agonistic activity of RBE as a preventive and therapeutic agent in the treatment of the neuro-inflammation associated with AD.</description><subject>Aged</subject><subject>Agonists</subject><subject>Alzheimer Disease - drug therapy</subject><subject>Alzheimer Disease - metabolism</subject><subject>Alzheimer's disease</subject><subject>Animals</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>CD163 antigen</subject><subject>CD36 antigen</subject><subject>CD45 antigen</subject><subject>Chemical compounds</subject><subject>Cognitive ability</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Lipopolysaccharides</subject><subject>Male</subject><subject>Markers</subject><subject>Metabolic Diseases</subject><subject>Mice</subject><subject>Microglia - metabolism</subject><subject>Modulation</subject><subject>Neurodegeneration</subject><subject>Neurodegenerative diseases</subject><subject>Neurology</subject><subject>Neurosciences</subject><subject>Oncology</subject><subject>Original Article</subject><subject>Oryza - metabolism</subject><subject>Peroxisome proliferator-activated receptors</subject><subject>Phagocytes</subject><subject>Pharmacology</subject><subject>Phenotypes</subject><subject>Pioglitazone</subject><subject>Plant Extracts - pharmacology</subject><subject>PPAR gamma - agonists</subject><subject>PPAR gamma - metabolism</subject><subject>Proteins</subject><subject>Receptors</subject><subject>Rice bran</subject><subject>Tau protein</subject><subject>Thiazolidinediones - therapeutic use</subject><issn>0885-7490</issn><issn>1573-7365</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kMtO3DAUhi1UBFPaF-iistR12uNL4mSJEJdKI3WEYG05zsmMURJP7UQCxILX6Ov1SXA6U9ixsL3w_39H5yPkC4PvDED9iIwBYxnwdEBJlskDsmC5EpkSRf6BLKAs80zJCo7JxxjvAEDkrDoix0KCFIwXC_K08jG6ukMafLp8S4OzSOtgBor3YzB2pG6gvbPBrztnOtr7ZurM6PxAx03w03pDV6vT62xt-t7QgBa3ow9xbpnucYOux_D3-U-kjYtoIs4snCnYfSKHrekift6_J-T24vzm7Cpb_rr8eXa6zKxQ-ZgVFSsVa1BVyJq2hLKwpallywvbIBouLedKytbkqqjaStUcrQLBWAU51A2KE_Jtx90G_3vCOOo7P4UhjdQ8VxyU4qVKKb5LpVVjDNjqbXC9CQ-agZ6F651wnYTrf8K1TKWve_RU99i8Vv4bTgGxC8T0NawxvM1-B_sCMmCNew</recordid><startdate>20211001</startdate><enddate>20211001</enddate><creator>El-Din, Shimaa Saad</creator><creator>Abd Elwahab, Sahar</creator><creator>Rashed, Laila</creator><creator>Fayez, Salwa</creator><creator>Aboulhoda, Basma Emad</creator><creator>Heikal, Ola Ahmed</creator><creator>Galal, Asmaa Fathi</creator><creator>Nour, Zeinab A.</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TK</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><orcidid>https://orcid.org/0000-0002-6101-8402</orcidid></search><sort><creationdate>20211001</creationdate><title>Possible role of rice bran extract in microglial modulation through PPAR-gamma receptors in alzheimer’s disease mice model</title><author>El-Din, Shimaa Saad ; Abd Elwahab, Sahar ; Rashed, Laila ; Fayez, Salwa ; Aboulhoda, Basma Emad ; Heikal, Ola Ahmed ; Galal, Asmaa Fathi ; Nour, Zeinab A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-691871de79e1df8086c8ab4f26cdeea24c22744fa5769f97b2ec703119050bde3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Aged</topic><topic>Agonists</topic><topic>Alzheimer Disease - drug therapy</topic><topic>Alzheimer Disease - metabolism</topic><topic>Alzheimer's disease</topic><topic>Animals</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>CD163 antigen</topic><topic>CD36 antigen</topic><topic>CD45 antigen</topic><topic>Chemical compounds</topic><topic>Cognitive ability</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Lipopolysaccharides</topic><topic>Male</topic><topic>Markers</topic><topic>Metabolic Diseases</topic><topic>Mice</topic><topic>Microglia - metabolism</topic><topic>Modulation</topic><topic>Neurodegeneration</topic><topic>Neurodegenerative diseases</topic><topic>Neurology</topic><topic>Neurosciences</topic><topic>Oncology</topic><topic>Original Article</topic><topic>Oryza - metabolism</topic><topic>Peroxisome proliferator-activated receptors</topic><topic>Phagocytes</topic><topic>Pharmacology</topic><topic>Phenotypes</topic><topic>Pioglitazone</topic><topic>Plant Extracts - pharmacology</topic><topic>PPAR gamma - agonists</topic><topic>PPAR gamma - metabolism</topic><topic>Proteins</topic><topic>Receptors</topic><topic>Rice bran</topic><topic>Tau protein</topic><topic>Thiazolidinediones - therapeutic use</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>El-Din, Shimaa Saad</creatorcontrib><creatorcontrib>Abd Elwahab, Sahar</creatorcontrib><creatorcontrib>Rashed, Laila</creatorcontrib><creatorcontrib>Fayez, Salwa</creatorcontrib><creatorcontrib>Aboulhoda, Basma Emad</creatorcontrib><creatorcontrib>Heikal, Ola Ahmed</creatorcontrib><creatorcontrib>Galal, Asmaa Fathi</creatorcontrib><creatorcontrib>Nour, Zeinab A.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Psychology Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><jtitle>Metabolic brain disease</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>El-Din, Shimaa Saad</au><au>Abd Elwahab, Sahar</au><au>Rashed, Laila</au><au>Fayez, Salwa</au><au>Aboulhoda, Basma Emad</au><au>Heikal, Ola Ahmed</au><au>Galal, Asmaa Fathi</au><au>Nour, Zeinab A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Possible role of rice bran extract in microglial modulation through PPAR-gamma receptors in alzheimer’s disease mice model</atitle><jtitle>Metabolic brain disease</jtitle><stitle>Metab Brain Dis</stitle><addtitle>Metab Brain Dis</addtitle><date>2021-10-01</date><risdate>2021</risdate><volume>36</volume><issue>7</issue><spage>1903</spage><epage>1915</epage><pages>1903-1915</pages><issn>0885-7490</issn><eissn>1573-7365</eissn><abstract>Alzheimer's Disease (AD), the most prevalent neurodegenerative disorder among elderly people, is ordinarily associated with progressive cognitive decline. Peroxisome proliferator-activated receptors-gamma (PPAR-γ) agonists can be targeted as a beneficial therapeutic strategy against AD. In the present study, we aimed to investigate the preventive and therapeutic effects of rice bran extract (RBE) as a possible PPAR-γ agonist on the microglial phenotype modulation in AD in mice compared to the effects of pioglitazone. This study included 64 adult male Swiss Albino mice divided into 8 groups, each group comprised 8 mice; control group, RBE group, lipopolysaccharide-induced neurodegeneration (a) (LPSa) group, (LPSb) group, RBE-preventive group (RBE + LPSa), pioglitazone-preventive group (PG + LPSa), RBE-treated group (RBE + LPSb), and pioglitazone-treated group (PG + LPSb). Cognitive functions were assessed by Y-maze and Morris water maze tests. The expression of PPAR-γ, CD45, arginase1, CD36, and CD163 genes was assessed by real time qPCR and the estimation of NF-kβ protein level was done by Western blot technique. Moreover, the assessment of Aβ42 and P-tau levels was performed by ELISA. Histopathological examination of brain tissues was performed for all the studied groups. Our results showed that RBE and pioglitazone could modulate microglial phenotype from M1 to M2 where they significantly decreased the expression of NF-κβ and the pro-inflammatory microglial marker (CD45) in parallel with increasing the expression of the anti-inflammatory microglial and phagocytic markers (arginase1, CD163, and CD36). In addition, RBE and pioglitazone significantly increased PPAR-γ expression and reduced Aβ42 deposition as well as p-tau protein levels. In conclusion, our study identified the possible role of PPAR-γ agonistic activity of RBE as a preventive and therapeutic agent in the treatment of the neuro-inflammation associated with AD.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>34043126</pmid><doi>10.1007/s11011-021-00741-4</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0002-6101-8402</orcidid></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0885-7490 |
| ispartof | Metabolic brain disease, 2021-10, Vol.36 (7), p.1903-1915 |
| issn | 0885-7490 1573-7365 |
| language | eng |
| recordid | cdi_proquest_journals_2572077287 |
| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| subjects | Aged Agonists Alzheimer Disease - drug therapy Alzheimer Disease - metabolism Alzheimer's disease Animals Biochemistry Biomedical and Life Sciences Biomedicine CD163 antigen CD36 antigen CD45 antigen Chemical compounds Cognitive ability Humans Inflammation Lipopolysaccharides Male Markers Metabolic Diseases Mice Microglia - metabolism Modulation Neurodegeneration Neurodegenerative diseases Neurology Neurosciences Oncology Original Article Oryza - metabolism Peroxisome proliferator-activated receptors Phagocytes Pharmacology Phenotypes Pioglitazone Plant Extracts - pharmacology PPAR gamma - agonists PPAR gamma - metabolism Proteins Receptors Rice bran Tau protein Thiazolidinediones - therapeutic use |
| title | Possible role of rice bran extract in microglial modulation through PPAR-gamma receptors in alzheimer’s disease mice model |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-07T08%3A34%3A18IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Possible%20role%20of%20rice%20bran%20extract%20in%20microglial%20modulation%20through%20PPAR-gamma%20receptors%20in%20alzheimer%E2%80%99s%20disease%20mice%20model&rft.jtitle=Metabolic%20brain%20disease&rft.au=El-Din,%20Shimaa%20Saad&rft.date=2021-10-01&rft.volume=36&rft.issue=7&rft.spage=1903&rft.epage=1915&rft.pages=1903-1915&rft.issn=0885-7490&rft.eissn=1573-7365&rft_id=info:doi/10.1007/s11011-021-00741-4&rft_dat=%3Cproquest_cross%3E2572077287%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2572077287&rft_id=info:pmid/34043126&rfr_iscdi=true |